Akademik Veri Yönetim Sistemi
HUMAN & EXPERIMENTAL TOXICOLOGY, cilt.22, sa.3, ss.155-158, 2003 (SCI-Expanded)
Seventy Swiss albino mice (6-week-old male) were selected for the investigation into aflatoxin B-1's role in the cause of kwashiorkor. The mice were divided randomly into four groups. They were grouped within each group by being fed either low or normal protein level diets supplemented with very small amounts of aflatoxin B-1 (0.5 mug/day). The control groups were fed aflatoxin B-1-free diets containing either normal or low protein levels. All groups were monitored for 7 weeks. The increase in body weight was found to be low in groups I and II, given diets contaminated with aflatoxin B,. Although groups II and IV, which were given low dietary protein, showed remarkable decreases in serum total protein and albumin levels (group 11: total protein 4.1 +/- 0.1 g/dL, albumin 2.6 +/- 0.8 g/dL and group IV: total protein 4.6 +/- 1.3 g/dL, albumin 2.8 +/- 0.82 g/dL) when compared with the groups fed a normal dietary protein level (group I: total protein 5.9 +/- 1.3 g/dL, albumin 3.4 +/- 0.7 g/dL and group III: total protein 5.4 +/- 1.6 g/dL, albumin 3.5 +/- 1.2 g/dL; P < 0.05). The statistical difference between these two groups was found not to be significant (P > 0.05). However, decreases in total protein and albumin levels were a little more prominent in group II. In addition, histopatological changes of the liver was remarkable in the group fed a low protein diet and aflatoxin B-1 when compared with the group fed only a low protein diet and no aflatoxin B-1. More significantly, however, was the increase in liver weight in both groups fed a low protein diet (groups 11 and IV). Our conclusion is that aflatoxin B-1 could not have contributed to the development of kwashiorkor.